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Biomimetic lithography and deposition kinetics of iron oxyhydroxide thin films

Description: Heterogeneous nucleation and crystal growth on functionalized organic substrates is a critical step in biological hard tissue formation. Self assembled monolayers can be derivatized with various organic functional groups to mimic the ``nucleation proteins`` for induction of mineral growth. Studies of nucleation and growth on SAMs can provide a better understanding of biomineralization and can also form the basis of a superior thin film deposition process. We demonstrate that micron-scale, electron and ion beam, lithographic techniques can be used to pattern SAMs with functional organic groups that either inhibit or promote mineral deposition. Patterned films of iron oxyhydroxide were deposited on the areas patterned with nucleation sites. Studies of the deposition kinetic of these films show that indeed the surface induces heterogeneous nucleation and that film formation does not occur via absorption of polymers or colloidal material formed homogeneously in solution. The nucleus interfacial free energy was calculated to be 24 mJ/m2 on a SAM surface composed entirely of sulfonate groups.
Date: December 1, 1993
Creator: Rieke, P. C.; Wood, L. L.; Marsh, B. M.; Fryxell, G. E.; Engelhard, M. H.; Baer, D. R. et al.
Partner: UNT Libraries Government Documents Department

Radiogenic neoplasia in thyroid and mammary clonogens. Final progress report, 1 January 1987--31 December 1997

Description: The induction of cancer by ionizing radiation is a matter of great practical importance to the nuclear industry, to national defense, to radiological medicine and to the general public. It is increasingly apparent that carcinogenesis is a leading dose-limiting effect of radiation exposure. The thyroid and mammary glands are among the most sensitive human tissues to radiogenic initiation of cancer, and there is a profoundly higher risk of neoplastic initiation in these glands among individuals irradiated before or during puberty than among those exposed in later life. The authors developed unique quantitative experimental models to investigate and characterize the cells of origin of thyroid and mammary cancers and the effects of radiation on them (C185). To study these progenitor cells in vivo it is necessary to have a system by which their concentrations, total numbers and responses to radiation and other factors can be measured. It is a truism that not all cells in a tissue are equally sensitive to neoplastic initiation. They reasoned that the progenitor cells are most likely members of that subpopulation that is necessary to maintenance of normal tissue cell numbers and to repair and replacement after tissue damage. They further reasoned that such cells would likely be responsive to specific mitogenic stimulation by hormones. On the basis of these considerations, they developed quantitative rat thyroid and mammary epithelial cell transplantation systems.
Date: July 10, 1998
Creator: Clifton, K.H.
Partner: UNT Libraries Government Documents Department

Time-specific measurements of energy deposition from radiation fields in simulated sub-micron tissue volumes

Description: A tissue-equivalent spherical proportional counter is used with a modified amplifier system to measure specific energy deposited from a uniform radiation field for short periods of time ({approximately}1 {micro}s to seconds) in order to extrapolate to dose in sub-micron tissue volumes. The energy deposited during these time intervals is compared to biological repair processes occurring within the same intervals after the initial energy deposition. The signal is integrated over a variable collection time which is adjusted with a square-wave pulse. Charge from particle passages is collected on the anode during the period in which the integrator is triggered, and the signal decays quickly to zero after the integrator feedback switch resets; the process repeats for every triggering pulse. Measurements of energy deposited from x rays, {sup 137}Cs gamma rays, and electrons from a {sup 90}Sr/{sup 90}Y source for various time intervals are taken. Spectral characteristics as a function of charge collection time are observed and frequency plots of specific energy and collection time-interval are presented. In addition, a threshold energy flux is selected for each radiation type at which the formation of radicals (based on current measurements) in mammalian cells equals the rate at which radicals are repaired.
Date: July 7, 1997
Creator: Famiano, M.A.
Partner: UNT Libraries Government Documents Department

Relevance of photobiological repair

Description: From symposium on new trends in photobiology; Rio de Janeiro, Brazil (15 Jul 1973). A review is presented of photobiological and photochemical studies in relation to radiation damage and repair. Some topics discussed are: repair of damage induced in DNA by ultraviolet and gamma radiation; the repair of chemically induced damage to DNA; uv-induced skin cancer; enzymic photoreactivation of uv-irradiated DNA; and phoioreactivation of uv-induced tumors in fish. (HLW)
Date: January 1, 1973
Creator: Setlow, R.B.
Partner: UNT Libraries Government Documents Department

Repair of human DNA: radiation chemical damage in normal and xeroderma pigmentosum cells

Description: The photolysis of bromodeoxyuridine (BrdUrd) incorporated during repair was used for the assay of DNA repair in human cells. This assay supplies a characterization of the sequence of repair events that occur in human cells after radiation exposure, both ultraviolet and ionizing, and permits an estimation of the size of the average repaired region after these physical insults to DNA. Chemical insults to DNA are discussed and an attempt is made to liken the repair processes after chemical damages of various kinds to those repair processes that occur in human DNA after damage from physical agents. Results are reported indicating that, under certain conditions, repair events resembling those seen after uv radiation can be observed in normal human cells after ionizing radiation and that xeroderma pigmentosum cells, defective in the repair of uv-induced DNA damage, show defective repair of these uv-like DNA lesions induced by ionizing radiation. (CH)
Date: January 1, 1974
Creator: Regan, J. D. & Setlow, R. B.
Partner: UNT Libraries Government Documents Department

Modeling of endovascular patch welding using the computer program LATIS

Description: A new computer program, LATIS, being developed at Lawrence Livermore National Laboratory is used to study the effect of pulsed laser irradiation on endovascular patch welding. Various physical and biophysical effects are included in these simulations: laser light scattering and absorption, tissue heating and heat conduction, vascular cooling, and tissue thermal damage. The geometry of a patch being held against the inner vessel wall (500 {mu}m inner diameter) by a balloon is considered. The system is exposed to light pulsed from an optical fiber inside the balloon. A minimum in the depth of damage into the vessel wall is found. The minimum damage zone is about the thickness of the patch material that is heated by the laser. The more ordered the tissue the thinner the minimum zone of damage. The pulse length which minimizes the zone of damage is found to be the time for energy to diffuse across the layer. The delay time between the pulses is determined by the time for the heated layer to cool down. An optimal pulse length exists which minimizes the total time needed to weld the patch to the wall while keeping the thickness of the damaged tissue to less than 100 {mu}m. For the case that is considered, a patch dyed with light absorbing ICG on the side next to the vessel (thickness of the dyed layer is 60 {mu}m), the best protocol is found to be 65-200 ms pulses applied over 2 min.
Date: March 1, 1995
Creator: Glinsky, M.E.; London, R.A.; Zimmerman, G.B. & Jacques, S.L.
Partner: UNT Libraries Government Documents Department

The construction of a physical map for human chromosome 19

Description: Unlike a genetic map which provides information on the relative position of genes or markers based upon the frequency of genetic recombination, a physical map provides a topographical picture of DNA, i.e. distances in base pairs between landmarks. The landmarks may be genes, gene markers, anonymous sequences, or cloned DNA fragments. Perhaps the most useful type of physical map is one that consists of an overlapping set of cloned DNA fragments (contigs) that span the chromosome. Once genes are assigned to this contig map, sequencing of the genomic DNA can be prioritized to complete the most interesting regions first. While, in practice, complete coverage of a complex genome in recombinant clones may not be possible to achieve, many gaps in a clone map may be closed by using multiple cloning vectors or uncloned large DNA fragments such as those separated by electrophoretic methods. Human chromosome 19 contains about 60 million base pairs of DNA and represents about 2% of the haploid genome. Our initial interest in chromosome 19 originated from the presence of three DNA repair genes which we localized to a region of this chromosome. Our approach to constructing a physical map of human chromosome 19 involves four steps: building a foundation of overlapping cosmid contigs; bridging the gaps in the cosmid map with hybridization-based methods to walk onto DNA cloned in yeast and cosmids: orienting the contigs relative to each other and linking them to the cytological map; and coupling the contig map with the genetic map. The methods we use and the current status of the map are summarized in this report. 6 refs., 1 fig.
Date: November 5, 1990
Creator: Carrano, A.V.; Alleman, J.; Amemiya, C.; Ashworth, L.K.; Aslanidis, C.; Branscomb, E.W. et al.
Partner: UNT Libraries Government Documents Department

[Nonhomologous mechanisms of repair of chromosomal breaks]. Progress report

Description: Broken chromosomes must either be repaired or lost. The break separates part of the chromosome, containing a telomere, from the rest, containing a centromere. While the centromerecontaining fragment can properly segregate, the broken end will be progressively degraded. The acentric fragment cannot segregate and will also be degraded. We have centered our attention on two alternative non-homologous mechanisms of repair: (1) the acquisition of a new telomere, and (2) repair of broken chromosomes by non-homologous joining of broken chromosome ends. In both cases, we create a double-strand break at a defined chromosomal location in yeast cells. The break is created by the site-specific HO endonuclease in cells that carry the rad52 mutation to prevent repair of a double-strand break by homologous recombination. In diploid cells, we can recover cells that contain a terminally deleted, healed chromosome that has acquired a new telomere. In haploid cells, we can recover cells in which the double-strand break has been repaired by rejoining the broken ends, usually accompanied by a deletion.
Date: September 1, 1993
Creator: Haber, J. E.
Partner: UNT Libraries Government Documents Department

Hematopoietic tissue repair under chronic low daily dose irradiation

Description: The capacity of the hematopoietic system to repair constantly accruing cellular damage under chronic, low daily dose gamma irradiation is essential for the maintenance of a functional hematopoietic system, and, in turn, long term survival. In certain individuals, however, such continuous cycles of damage and repair provide an essential inductive environment for selected types of hematopathologies, e.g., myeloid leukemia (ML). We have been studying temporal and causal relationships between hematopoietic capacity, associated repair functions, and propensities for hematologic disease in canines under variable levels of chronic radiation stress (0.3{minus}26.3 cGy d{sup {minus}1}). Results indicate that the maximum exposure rate tolerated by the hematopoietic system is highly individual-specific and is based largely on the degree to which repair capacity, and, in turn, hematopoietic restoration, is augmented under chronic exposure. In low-tolerance individuals (prone to aplastic anemia, subgroup (1), the failure to augment basic m-pair functions seemingly results in a progressive accumulation of genetic and cellular damage within vital progenitorial marrow compartments particularly marked within erythroid compartments. that results in loss of reproductive capacity and ultimately in collapse of the hematopoietic system. The high-tolerance individuals (radioaccomodated and either prone- or not prone to ML, subgroup 2 & 3 appear to minimize the accumulating damage effect of daily exposures by extending repair functions, which preserves reproductive integrity and fosters regenerative hematopoietic responses. As the strength of the regenerative response manifests the extent of repair augmentation, the relatively strong response of high- tolerance individuals progressing to patent ML suggests an insufficiency of repair quality rather than repair quantity.
Date: December 1, 1994
Creator: Seed, T. M.
Partner: UNT Libraries Government Documents Department

Report on NCI symposium: comparison of mechanisms of carcinogenesis by radiation and chemical agents. II. Cellular and animal models

Description: The point at which the common final pathway for induction of cancer by chemical carcinogens and ionizing radiation has not been identified. Although common molecular targets are suggested by recent findings about the role of oncogenes, the mechanism by which the deposition of radiation energy and the formation of adducts or other DNA lesions induced by chemicals affects the changes in the relevant targets may be quite different. The damage to DNA that plays no part in the transformation events, but that influences the stability of the genome, and therefore, the probability of subsequent changes that influence tumorigenesis may be more readily induced by some agents than others. Similarly, the degree of cytotoxic effects that disrupt tissue integrity and increase the probability of expression of initiated cells may be dependent on the type of carcinogen. Also, evidence was presented that repair of the initial lesions could be demonstrated after exposure to low-LET radiation but not after exposure to chemical carcinogens.
Date: January 1, 1984
Creator: Fry, R.J.M.
Partner: UNT Libraries Government Documents Department

DNA damage in mammalian cells and its relevance to lethality

Description: From fourth symposium on microdosimetry; Pallanza, Italy (24 Sep 1973). Cell killing (loss of proliferative capacity) is a principal end point in all radiation effects contingent upon cell viability. DNA, the molecular carrier of the genetic inheritance, affects the affairs of a cell because the properties and characteristics of a cell are dictated by the DNA -- RNA -- protein axis of information storage, flow, and expression. Thus, the mutagenic and chromosome- breaking properties of radiation, the biological amplification available to a lesion in DNA, and the fact that DNA molecularly constitutes a very large radiation target, aH make DNA the principal target relative to many radiation effects. An indirect approach may be useful in studies of the sensitive targets in a mammalian cell. This stems from the fact that to kill cells with low LET radiation; sublethal damage must be accumulated and cells can repair this damage. Thus, focussing on DNA, and repair processes in DNA, while indirect, is supporied in the instance of cell killing by extensive experimental evidence. The status of damage registered directly in DNA may be assessed by examining changes in the sedimentation of DNA from irradiated cells. Along with measurements of cell survival, sedimentation data are discussed relative to their bearing on cell killing and their ability to help us understand the organization and replication of DNA in mammalian cells. (CH)
Date: January 1, 1973
Creator: Elkind, M.M. & Ben-Hur, E.
Partner: UNT Libraries Government Documents Department